Erythrovirus B19 infection in acquired immunodeficiency syndrome: screening by histopathology, immunohistochemistry, and in situ hybridization

Abstract

Erythrovirus B19 infects erythrocytic progenitors, transiently interrupting erythropoiesis. In AIDS patients it causes chronic anemia amenable to treatment. We looked for evidences of B19 infection in stored bone marrow material from patients with acquired immunodeficiency syndrome. Histological sections were made from stored paraffin blocks from 33 autopsies (39 blocks) and 35 biopsies (45 blocks, 30 patients) performed from 1988 to 2002. They were examined after hematoxylin-eosin (HE) staining, immunohistochemical (IHC), and in situ hybridization. HE revealed intra-nuclear inclusion bodies ("lantern cells") suggesting B19 infection in 19 sections corresponding to 19 of 63 patients examined with this test. Seven of 78 sections subjected to immunohistochemistry were positive, corresponding to 7 of 58 patients examined with this test. Fourteen sections corresponding to 13 of the 20 HE and/or IHC positive patients were subjected to in situ hybridization, with six positives results. Among the 13 patients subjected to the three techniques, only one gave unequivocal positive results in all and was considered a true positive. The frequency of B19 infection (1/63 patients) in the material examined can be deemed low.Key words: parvovirus B19-anemia -chronic-immunodeficiency Erythrovirus B19 infects human erythrocytic progenitor cells, leading to a transient interruption of erythropoiesis. In the immunocompetent host this viral infection is cleared within two weeks as a result of the appearance of serum specific antibodies, and the hematological manifestations are restricted to a slight and asymptomatic decline in the hemoglobin levels. When the antibodies appear there may be symptoms of immune complex disease like arthralgias and exanthema. This is what normally takes place during the common childhood exanthematic disease erythema infectiosum. The course can be quite different in certain kinds of host, like those with hereditary hemolytic anemias (e.g., sickle-cell anemia), in whom an acceptable hematocrit is maintained only through an intense and uninterrupted bone marrow activity. In this context erythrovirus B19 infection usually leads to the rapid onset of a life threatening acute anemia, the so called "transient aplastic crisis". The patient is transfusion-dependent until the appearance of specific antibodies spontaneously clears the infection. A similar situation can be found in the fetus, where normal erythron volume expansion also demands a high activity of the hematopoietic fetal tissues. The sudden interruption of hematopoiesis leads to fetal heart failure and anasarca (hydrops fetalis), which may result in fetal death. In immunocompromised individuals (e.g., HIV-infected patients) erythrovirus infection is not readily cleared and its long persistence leads to chronic anemia. In these patients, intravenous standard immunoglobulin infusions usually end viremia and restore hematopoiesis (de Mayolo & Temple 1990, Mitchell et al. 1990, Gottlieb & Deutsch 1992, Noronha et al. 2005.Erythrovirus B19 was discovered by...

Parvovirus Infection: An Immunohistochemical Study Using Fetal and Placental Tissue

“…Histologic sections of infected fetal tissue show typical intranuclear, brick-red inclusion in normoblasts. In situ hybridization to viral DNA [4,[6][7][8], and IHC using antibodies against VP1 and/or VP2 viral proteins [1,2] can also be used to diagnose infection in histologic sections.…”